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<p>Chronic stress is a major cause of affective pathogenesis, such as anxiety and depression. Experimental animal models, including rodents and zebrafish, are a valuable tool for translational neuroscience research focusing on stress-related brain disorders. Here, we examined the effects of 5- and 12-week chronic unpredictable stress (CUS5 and CUS12) on zebrafish behavior, whole-body cortisol and neuroinflammation-related biomarker gene expression, including markers of pro-inflammatory microglia (<i>NOS2a, COX2, P75NTR</i>) and astroglia (<i>C3, GBP</i>), and markers of anti-inflammatory microglia (<i>ARG-1, CD206</i>) and astroglia (<i>S100a10, PTX</i>). We also assessed stress-induced changes in brain monoamine levels and brain-blood-barrier permeability. Overall, CUS5 induced anxiety-like behavior, accompanied by elevated CNS pro-inflammatory marker gene&#xa0;expression, cortisol signaling and norepinephrine levels. In contrast, CUS12 induced depression-like behavior, accompanied by lowered cortisol levels, impaired serotonin turnover and activated anti-inflammatory biomarker gene expression, as well as upregulated histone deacetylase 4 gene (suggesting the involvement of epigenetic regulation). Collectively, this confirms the importance of stress duration as a key&#xa0;factor in the development of stress-related disorders in zebrafish models, and further&#xa0;implicates pro- and inti-inflammatory neuroglia in affective pathogenesis.</p>

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Prolonged 5-week and 12-week chronic stress differentially modulates CNS expression of pro- and anti-neuroinflammatory biomarkers, brain monoamines and affective behavior in adult zebrafish

  • 期刊论文

  • 发表日期：

    2025年4月12日

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  • Maria M. Kotova,
  • Sahil V. Amikishiev,
  • Kirill V. Apukhtin,
  • David S. Galstyan,
  • Murilo S. de Abreu,
  • Adam Michael Stewart,
  • Longen Yang,
  • Allan V. Kalueff

摘要

Chronic stress is a major cause of affective pathogenesis, such as anxiety and depression. Experimental animal models, including rodents and zebrafish, are a valuable tool for translational neuroscience research focusing on stress-related brain disorders. Here, we examined the effects of 5- and 12-week chronic unpredictable stress (CUS5 and CUS12) on zebrafish behavior, whole-body cortisol and neuroinflammation-related biomarker gene expression, including markers of pro-inflammatory microglia (NOS2a, COX2, P75NTR) and astroglia (C3, GBP), and markers of anti-inflammatory microglia (ARG-1, CD206) and astroglia (S100a10, PTX). We also assessed stress-induced changes in brain monoamine levels and brain-blood-barrier permeability. Overall, CUS5 induced anxiety-like behavior, accompanied by elevated CNS pro-inflammatory marker gene expression, cortisol signaling and norepinephrine levels. In contrast, CUS12 induced depression-like behavior, accompanied by lowered cortisol levels, impaired serotonin turnover and activated anti-inflammatory biomarker gene expression, as well as upregulated histone deacetylase 4 gene (suggesting the involvement of epigenetic regulation). Collectively, this confirms the importance of stress duration as a key factor in the development of stress-related disorders in zebrafish models, and further implicates pro- and inti-inflammatory neuroglia in affective pathogenesis.